Work continues on the sympathetic neuro-effector junction in vascular smooth muscle. Studies in progress include: 1. The changes in reactivity of saphenous veins to small decrease in extracellular sodium. The evidence indicates that a decrease of extracellular sodium from the normal value of 143.3 to 131.1 mEq/1can enhance the response of the venous smooth muscle to adrenergic stimuli. 2. The interaction is being examined between the activation of pre-junctional alpha-adrenergic receptors in vascular smooth muscle and spleen and the neuronal amine uptake mechanism for norepinephrine 3. The mechanism by which isoproterenol causes relaxation in vascular smooth muscle is under study. Preliminary experiments indicate that isoprterenol reduces the influx of extracellular Ca ions through 1 "channel" which is independent of sustained membrane depolarization. 4. The activity of the cardiac glycosides to cause transmitter release from sympathetic nerve ending in the heart and blood vessels is being tested. From initial studies it seems that the glycosides can cause release of norepinephrine by a process which can be initiated in the absence of Ca ions and which involves alpha adrenoceptors on the sympathetic nerve terminals.